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What Causes Kussmaul Respirations In Dka?

Respiratory System And Diabetes

Respiratory System And Diabetes

Tweet The respiratory system is the system of organs that allow the body to take in oxygen and expel carbon dioxide, this process is known as gaseous exchange. We generally breathe between 12 and 20 times a minute. There are a number of complications of diabetes that can negatively affect our breathing. Parts of the respiratory system The following parts of the body make up the respiratory system: Mouth and nose Trachea (windpipe) Lungs Diaphragm How the respiratory system works Breathing is usually initiated by contraction of the diaphragm, a muscle which separates the chest cavity from the abdomen. Tweet Type 2 diabetes mellitus is a metabolic disorder that results in hyperglycemia (high blood glucose levels) due to the body: Being ineffective at using the insulin it has produced; also known as insulin resistance and/or Being unable to produce enough insulin Type 2 diabetes is characterised by the body being unable to metabolise glucose (a simple sugar). This leads to high levels of blood glucose which over time may damage the organs of the body. From this, it can be understood that for someone with diabetes something that is food for ordinary people can become a sort of metabolic poison. This is why people with diabetes are advised to avoid sources of dietary sugar. The good news is for very many people with type 2 diabetes this is all they have to do to stay well. If you can keep your blood sugar lower by avoiding dietary sugar, likely you will never need long-term medication. Type 2 diabetes was formerly known as non-insulin-dependent or adult-onset diabetes due to its occurrence mainly in people over 40. However, type 2 diabetes is now becoming more common in young adults, teens and children and accounts for roughly 90% of all diabetes cases worldwide. How serious Continue reading >>

Nursing Management Of A Patient With Diabetic Ketoacidosis Nursing Essay

Nursing Management Of A Patient With Diabetic Ketoacidosis Nursing Essay

Disclaimer: This essay has been submitted by a student. This is not an example of the work written by our professional essay writers. Any opinions, findings, conclusions or recommendations expressed in this material are those of the authors and do not necessarily reflect the views of UK Essays. David (18 years, male) is suffering from a condition known as 'diabetic ketoacidosis'. This is a very serious condition that occurs in diabetes where the body is unable to use the blood glucose to meet the energy needs due to the lack of insulin in the body. Therefore the body utilizes fat and the breakdown of fats results in the formation of ketones which slowly build up in the body could be toxic. Usually, Insulin plays a major role in the manner in which glucose is utilized as an energy source (Mayo 2010). With a lack of insulin, glucose does not enter the blood cells and hence fat is utilized as an alternative energy source. Any type of diabetes is at the risk of developing diabetic ketoacidosis (especially type 1, & rare case in type 2), and this condition often requires emergency and critical care. Diabetic ketoacidosis is associated with certain risk factors such as illness, problems with insulin therapy, excessive stress, emotional or physical trauma, recent surgery, tremors, heart attack, listlessness, stroke, drug or alcohol abuse (Margaret, 2006). Type 2 diabetics can develop diabetic ketoacidosis following a bout of serious infection. Individuals who are Hispanic or African-American in origin are at a higher risk of developing diabetic ketoacidosis following type 2 diabetes. David is 18 years old and has developed diabetes ketoacidosis as a complication of type 1 diabetes (more likely) or type 2 diabetes (very rare), and this complication is common in this age/disease Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) is a serious problem that can occur in people with diabetes if their body starts to run out of insulin. This causes harmful substances called ketones to build up in the body, which can be life-threatening if not spotted and treated quickly. DKA mainly affects people with type 1 diabetes, but can sometimes occur in people with type 2 diabetes. If you have diabetes, it's important to be aware of the risk and know what to do if DKA occurs. Symptoms of diabetic ketoacidosis Signs of DKA include: needing to pee more than usual being sick breath that smells fruity (like pear drop sweets or nail varnish) deep or fast breathing feeling very tired or sleepy passing out DKA can also cause high blood sugar (hyperglycaemia) and a high level of ketones in your blood or urine, which you can check for using home-testing kits. Symptoms usually develop over 24 hours, but can come on faster. Check your blood sugar and ketone levels Check your blood sugar level if you have symptoms of DKA. If your blood sugar is 11mmol/L or over and you have a blood or urine ketone testing kit, check your ketone level. If you do a blood ketone test: lower than 0.6mmol/L is a normal reading 0.6 to 1.5mmol/L means you're at a slightly increased risk of DKA and should test again in a couple of hours 1.6 to 2.9mmol/L means you're at an increased risk of DKA and should contact your diabetes team or GP as soon as possible 3mmol/L or over means you have a very high risk of DKA and should get medical help immediately If you do a urine ketone test, a result of more than 2+ means there's a high chance you have DKA. When to get medical help Go to your nearest accident and emergency (A&E) department straight away if you think you have DKA, especially if you have a high level of ketones in Continue reading >>

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State

Acute hyperglycemia, or high blood glucose, may be either the initial presentation of diabetes mellitus or a complication during the course of a known disease. Inadequate insulin replacement (e.g., noncompliance with treatment) or increased insulin demand (e.g., during times of acute illness, surgery, or stress) may lead to acute hyperglycemia. There are two distinct forms: diabetic ketoacidosis (DKA), typically seen in type 1 diabetes, and hyperosmolar hyperglycemic state (HHS), occurring primarily in type 2 diabetes. In type 1 diabetes, no insulin is available to suppress fat breakdown, and the ketones resulting from subsequent ketogenesis manifest as DKA. This is in contrast to type 2 diabetes, in which patients can still secrete small amounts of insulin to suppress DKA, instead resulting in a hyperglycemic state predominated simply by glucose. The clinical presentation of both DKA and HHS is one of polyuria, polydipsia, nausea and vomiting, volume depletion (e.g., dry oral mucosa, decreased skin turgor), and eventually mental status changes and coma. In patients with altered mental status, fingerstick glucose should always be checked in order to exclude serum glucose abnormalities. Several clinical findings pertaining only to DKA include a fruity odor to the breath, hyperventilation, and abdominal pain. HHS patients, in contrast to those with DKA, will present with more extreme volume depletion. The treatment of both DKA and HHS is primarily IV electrolyte and fluid replacement. Insulin for hyperglycemia may be given with caution and under vigilant monitoring of serum glucose. Other treatment options depend on the severity of symptoms and include bicarbonate and potassium replacement. Osmotic diuresis and hypovolemia Hypovolemia resulting from DKA can lead to acute Continue reading >>

Diabetic Ketoacidosis And Patho

Diabetic Ketoacidosis And Patho

pathophysiology ketogenesis due to insulin deficiency leads to increased serum levels of ketones anad ketonuria acetoacetate, beta-hydroxybutyrate; ketone bodies produced by the liver, organic acids that cause metabolic acidosis respiration partially compensates; reduces pCO2, when pH < 7.2, deep rapid respirations (Kussmaul breathing) acetone; minor product of ketogenesis, can smell fruity on breath of ketoacidosis patients elevated anion gap Methanol intoxication Uremic acidosis Diabetic ketoacidosis Paraldehyde ingestions Intoxicants (salicyclate, ethylene glycol, nipride, epinephrine, norepinephrine) Lactic acidosis (drug induced; didanosine, iron, isoniazid, metformin, zidovudine) Ethanol ketoacidosis Severe renal failure starvation Blood glucose regulation (6) 1. When blood glucose levels rise above a set point, 2. the pancreas secretes insulin into the blood. 3. Insulin stimulates liver and muscle cells to make glycogen, dropping blood glucose levels. 4. When glucose levels drop below a set point, 5. the pancreas secretes glucagon into the blood. 6. Glucagon promotes the breakdown of glycogen and the release of glucose into the blood. (The pancreas signals distant cells to regulate levels in the blood = endocrine function.) Insulin and Glucagon (Regulation) (10) 1. High blood glucose 2. Beta cells 3. Insulin 4. Glucose enters cell 5. Blood glucose lowered 6. Low blood glucose 7. Alpha cells 8. Glucagon 9. Liver releases glucose from glycogen 10. Blood glucose raised What is the manifestations (symptoms) of Type 1? (10) 1. Extreme thirst 2. Frequent urination 3. Drowsiness, lethargy 4. Sugar in urine 5. Sudden vision change 6. Increased appetite 7. Sudden weight loss 8. Fruity, sweet, or wine like odor on breath 9. Heavy, laboured breathing 10. Stupor, unconscious Continue reading >>

Diabetic Ketoacidosis (dka)

Diabetic Ketoacidosis (dka)

Learning Objectives 1.Diagnosis of DKA 2.Precipitants of DKA 3.Managment of DKA 4. LADA- late onset autoimm. diabetes of adulthood DKA is most common in DM1 but can occur in DM2 when under significant stress. Normally, insulin allows tissue (mostly muscle) to take up glucose and suppresses lipolysis and proteolysis (anabolic state) When under stress and with insulin deficiency, the body produces glucagon-> glycogenolysis-> hi blood glucose and increases lipolysis-> FFA like beta hydroxybutyrate and acetoactone which cause acidosis(catabolic state) Lab abnormalities: hi bg (blood glucose), agap acidosis, ketonemia, ketonuria "serum ketone" tests measure acetoacetone, which is just one of the 2 major ketones serum b- hydroxybutyrate is a more accurate test of ketonemia but less readily available ketonuria can have false positive with some drugs ie) captopril K+ may be high in serum due to acidemia causing extracellular shifts, but pt have overall low K+ BUN and creatinine may reflect dehydration as glucosuria causes osmotic diuresis PE: fruity breath (acetone), kussmaul's respirations (deep labored), tachycardia, hypotension Triggers: Infection ie) influenza, pneumonia, gastroenterits Significant stressors: ACS, CVA, drugs (cocaine, meth) Noncompliance: insulin pump dysfunction, insulin noncompliance Will Daines gave us a nice tool: "6 i's"causing dka infection, ischemia, insulin deficiency, intra-abd processes (compromising pancreatic function), iatrogenic (ie) steroids), and ingestions (meth, cocaine) Management of DKA 1.Confirm diagnosis (plasma glucose, positive serum ketones, metabolic acidosis). 2.Admit to hospital; ICU may be necessary for frequent monitoring or if pH < 7.00 or AMS 3.Assess: Serum electrolytes (K+, Na+, Mg2+, Cl-, bicarbonate, phosphate) Acid-base Continue reading >>

Diabetic Ketoacidosis

Diabetic Ketoacidosis

Diabetes mellitus is the name given to a group of conditions whose common hallmark is a raised blood glucose concentration (hyperglycemia) due to an absolute or relative deficiency of the pancreatic hormone insulin. In the UK there are 1.4 million registered diabetic patients, approximately 3 % of the population. In addition, an estimated 1 million remain undiagnosed. It is a growing health problem: In 1998, the World Health Organization (WHO) predicted a doubling of the worldwide prevalence of diabetes from 150 million to 300 million by 2025. For a very tiny minority, diabetes is a secondary feature of primary endocrine disease such as acromegaly (growth hormone excess) or Cushing’s syndrome (excess corticosteroid), and for these patients successful treatment of the primary disease cures diabetes. Most diabetic patients, however, are classified as suffering either type 1 or type 2 diabetes. Type 1 diabetes Type 1 diabetes, which accounts for around 15 % of the total diabetic population, is an autoimmune disease of the pancreas in which the insulin-producing β-cells of the pancreas are selectively destroyed, resulting in an absolute insulin deficiency. The condition arises in genetically susceptible individuals exposed to undefined environmental insult(s) (possibly viral infection) early in life. It usually becomes clinically evident and therefore diagnosed during late childhood, with peak incidence between 11 and 13 years of age, although the autoimmune-mediated β-cell destruction begins many years earlier. There is currently no cure and type 1 diabetics have an absolute life-long requirement for daily insulin injections to survive. Type 2 diabetes This is the most common form of diabetes: around 85 % of the diabetic population has type 2 diabetes. The primary prob Continue reading >>

Kussmaul Breathing - An Overview | Sciencedirect Topics

Kussmaul Breathing - An Overview | Sciencedirect Topics

Nicholas J. White, in Manson's Tropical Infectious Diseases (Twenty-third Edition) , 2014 Hyperventilation or Kussmaul's breathing (sometimes termed respiratory distress) is a poor prognostic sign in malaria. In the tachypnoea associated with high fever, breathing is shallow compared with the ominous laboured hyperventilation associated with metabolic acidosis, pulmonary oedema or bronchopneumonia. Acute pulmonary oedema (acute respiratory distress syndrome) may develop at any time in severe falciparum malaria. It is particularly common in pregnant women, but rare in children. In some cases malaria ARDS may be difficult to distinguish clinically from pneumonia. The heart sounds are normal. The central venous pressure and pulmonary artery occlusion pressures are usually normal, the cardiac index is high and systemic vascular resistance is low. This points to an increase in capillary permeability (unless the patient has been overhydrated). The chest radiograph shows increased interstitial shadowing and a normal heart size. Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 Symptoms include nausea, vomiting, anorexia, polydipsia, and polyuria. Patients often exhibit Kussmaul respirations and volume depletion. Neurologic symptoms include fatigue and lethargy with depression of the sensorium. CSF exhibits a change in acid-base status with treatment of diabetic ketoacidosis. Even without bicarbonate administration, CSF pH falls as a result of the ventilatory response to the correction of acidosis and the sudden rise in Pco2. However, no correlation between decreased CSF pH and depression of sensorium has been established. Ketoacidosis is also seen in cases of starvation, in which it is generally mild and not associated with hyperglycemia. Ketoacids Continue reading >>

Kussmaul Breathing

Kussmaul Breathing

Not to be confused with Kussmaul's sign. Graph showing the Kussmaul breathing and other pathological breathing patterns. Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration. In metabolic acidosis, breathing is first rapid and shallow[1] but as acidosis worsens, breathing gradually becomes deep, labored and gasping. It is this latter type of breathing pattern that is referred to as Kussmaul breathing. Terminology[edit] Adolph Kussmaul, who introduced the term, referred to breathing when metabolic acidosis was sufficiently severe for the respiratory rate to be abnormal or reduced.[2] This definition is also followed by several other sources,[3][4] including for instance Merriam-Webster, which defines Kussmaul breathing as "abnormally slow deep respiration characteristic of air hunger and occurring especially in acidotic states".[5] Other sources, however, use the term Kussmaul respiration also when acidosis is less severe, in which case breathing is rapid.[4][6] Note that Kussmaul breathing occurs only in advanced stages of acidosis, and is fairly rarely reached. In less severe cases of acidosis, rapid, shallow breathing is seen. Kussmaul breathing is a kind of very deep, gasping, desperate breathing. Occasionally, medical literature refers to any abnormal breathing pattern in acidosis as Kussmaul breathing; however, this is inaccurate. History[edit] Kussmaul breathing is named for Adolph Kussmaul,[2] the 19th century German doctor who first noted it among patients with advanced diabetes mellitus. Kussm Continue reading >>

Dka Vs Hhs (hhns) Nclex Review

Dka Vs Hhs (hhns) Nclex Review

Diabetic ketoacidosis vs hyperglycemic hyperosmolar nonketotic syndrome (HHNS or HHS): What are the differences between these two complications of diabetes mellitus? This NCLEX review will simplify the differences between DKA and HHNS and give you a video lecture that easily explains their differences. Many students get these two complications confused due to their similarities, but there are major differences between these two complications. After reviewing this NCLEX review, don’t forget to take the quiz on DKA vs HHNS. Lecture on DKA and HHS DKA vs HHNS Diabetic Ketoacidosis Affects mainly Type 1 diabetics Ketones and Acidosis present Hyperglycemia presents >300 mg/dL Variable osmolality Happens Suddenly Causes: no insulin present in the body or illness/infection Seen in young or undiagnosed diabetics Main problems are hyperglycemia, ketones, and acidosis (blood pH <7.35) Clinical signs/symptoms: Kussmaul breathing, fruity breath, abdominal pain Treatment is the same as in HHNS (fluids, electrolyte replacement, and insulin) Watch potassium levels closely when giving insulin and make sure the level is at least 3.3 before administrating. Hyperglycemic Hyperosmolar Nonketotic Syndrome Affects mainly Type 2 diabetics No ketones or acidosis present EXTREME Hyperglycemia (remember heavy-duty hyperglycemia) >600 mg/dL sometimes four digits High Osmolality (more of an issue in HHNS than DKA) Happens Gradually Causes: mainly illness or infection and there is some insulin present which prevents the breakdown of ketones Seen in older adults due to illness or infection Main problems are dehydration & heavy-duty hyperglycemia and hyperosmolarity (because the glucose is so high it makes the blood very concentrated) More likely to have mental status changes due to severe dehydrat Continue reading >>

Diabetic Ketoacidosis: What It Is And How To Avoid It

Diabetic Ketoacidosis: What It Is And How To Avoid It

Diabetic ketoacidosis is a life threatening complication. It is common in people with Type 1 Diabetes because their pancreas does not produce insulin. But, it can also happen in individuals with Type 2 Diabetes when their blood sugar reaches critical level. During episodes of DKA, the body runs low on insulin so it burns fats as an alternative energy source. This process produces high level of ketone acids causing the following symptoms: Nausea Vomiting coffee-ground color Excessive thirst and urination Severe abdominal pain which may be cause by pancreatitis, GI tract perforation Kussmaul respiration (a deep and laborious breathing) Confusion Lethargy Dehydration Elevated heart rate (tachycardia) Comatose (severe cases) Blurring of the vision Fruity breath odor Diabetic ketoacidosis has four characteristics that result in the development of the symptoms: hyperglycemia, acidosis, dehydration, and electrolyte imbalance. During hyperglycemia, which causes the blurry vision, the glucose accumulates in the blood. The lack of insulin prevents glucose from entering the cells (hepatic glucose overproduction). The production of counter regulatory hormones such as catecholamines, cortisol, and glucagon, also increases. Gluconeogenesis and glycogenolysis take place. Insulin resistance increases during this stage. This makes it more difficult for the tissues to absorb glucose. The increase in counter-regulatory hormone levels and insulin resistance cause the release of glycerol and fatty acids. The liver starts oxidizing free fatty acids producing high levels of ketone acids. This process leads to ketoanemia. The ketone acids break down into hydrogen ions and ketone anions. The body then tries to bind the hydrogen ions by using up its alkali reserves causing acidosis. To address a Continue reading >>

Feline Endocrine Emergencies (proceedings)

Feline Endocrine Emergencies (proceedings)

1234Next Diabetic Ketoacidosis Diabetic ketoacidosis (DKA) is one of the most commonly encountered endocrine emergencies in small animal practice. DKA is typically seen in previously undiagnosed diabetics and less commonly occurs in patients that are on inadequate amounts of insulin. In patients currently receiving insulin, DKA is typically seen in those with a concurrent illness leading to insulin resistance. The pathogenesis of DKA is multifactorial; the four underlying causes include insulin deficiency, diabetogenic hormone excess (catecholamines, cortisol, glucagons, growth hormone), fasting, and dehydration. The interplay between these factors further antagonizes the situation. Clinical Findings Patients with DKA are divided into those that are "healthy" and those that are sick. Healthy DKAs only display clinical signs typical of diabetes (pu-pd, polyphagia, weight loss) and present without a history of vomiting, anorexia, or lethargy. Typically these patients have only trace-to-small amounts of ketonuria noted. Healthy DKA's can be treated like uncomplicated diabetics. Sick DKA patients have other systemic signs such as vomiting and lethargy. Physical exam findings may include depression, dehydration, weakness, tachypnea – this may progress to Kussmaul respiration (slow, deep breathing) due to acidosis and an acetone odor to the breath. It is not uncommon for patients in DKA to be presented semicomatose. These patients are true EMERGENCIES!!! Signs may reflect concurrent illnesses as well. Diagnosis DKA can be rapidly and easily diagnosed. The criteria for establishing this diagnosis include hyperglycemia, glucosuria, ketonuria, and metabolic acidosis. The presence of hyperglycemia which can be documented using a portable glucometer or point-of-care analyzer in Continue reading >>

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic Ketoacidosis: Evaluation And Treatment

Diabetic ketoacidosis is characterized by a serum glucose level greater than 250 mg per dL, a pH less than 7.3, a serum bicarbonate level less than 18 mEq per L, an elevated serum ketone level, and dehydration. Insulin deficiency is the main precipitating factor. Diabetic ketoacidosis can occur in persons of all ages, with 14 percent of cases occurring in persons older than 70 years, 23 percent in persons 51 to 70 years of age, 27 percent in persons 30 to 50 years of age, and 36 percent in persons younger than 30 years. The case fatality rate is 1 to 5 percent. About one-third of all cases are in persons without a history of diabetes mellitus. Common symptoms include polyuria with polydipsia (98 percent), weight loss (81 percent), fatigue (62 percent), dyspnea (57 percent), vomiting (46 percent), preceding febrile illness (40 percent), abdominal pain (32 percent), and polyphagia (23 percent). Measurement of A1C, blood urea nitrogen, creatinine, serum glucose, electrolytes, pH, and serum ketones; complete blood count; urinalysis; electrocardiography; and calculation of anion gap and osmolar gap can differentiate diabetic ketoacidosis from hyperosmolar hyperglycemic state, gastroenteritis, starvation ketosis, and other metabolic syndromes, and can assist in diagnosing comorbid conditions. Appropriate treatment includes administering intravenous fluids and insulin, and monitoring glucose and electrolyte levels. Cerebral edema is a rare but severe complication that occurs predominantly in children. Physicians should recognize the signs of diabetic ketoacidosis for prompt diagnosis, and identify early symptoms to prevent it. Patient education should include information on how to adjust insulin during times of illness and how to monitor glucose and ketone levels, as well as i Continue reading >>

What Is Kussmaul Breathing?

What Is Kussmaul Breathing?

Kussmaul breathing is a deep, labored breathing pattern that indicates that the body or organs have become too acidic. The body is constantly doing work to maintain an average temperature and neutral blood acidity. To make sure this balance happens; the kidneys and cells rely on bases or buffers, chemical compounds that bind with hydrogen ions. Disruptions to these compounds cause Kussmaul breathing, which is typically associated with conditions that cause metabolic disturbances, such as kidney failure and diabetes. Contents of this article: Kussmaul breathing is a type of hyperventilation that is the lung's emergency response to acidosis. Kussmaul breathing causes a labored, deeper breathing rate. It is most commonly associated with conditions that cause metabolic acidosis, particularly diabetes. Because Kussmaul breathing is a sign of severe metabolic acidosis, which is a life-threatening condition, hospitalization is usually necessary. What is Kussmaul breathing? When the body produces or ingests too much acid; or the kidneys or lungs are failing, blood acid levels increase. If the blood becomes too acidic, acidosis occurs, and the body takes action to restore the imbalance. By using deeper, longer breaths, the lungs can expel more acidic carbon dioxide (C02) than normal. The condition takes its name from Adolph Kussmaul, the German physician who first described the breathing pattern in 1874. Symptoms As a type of hyperventilation, some people describe Kussmaul breathing as panicked breathing, where someone appears to be gasping for breath. The deep, powerful breathing associated with Kussmaul breathing often causes inhalation and exhalation to become more evident and loud. Some compare the sound to exaggerated sighing. Symptoms of acidosis Before the deep and labore Continue reading >>

Pneumomediastinum As A Complication Of Diabetic Ketoacidosis

Pneumomediastinum As A Complication Of Diabetic Ketoacidosis

To the Editor: I read with interest the Chest Film Clinic on pneumomediastinum by Weinstock, Boiselle, and Roberts in the August issue (What caused this woman's pneumomediastinum? J Respir Dis. 2008;29:314-317). In the discussion of the differential diagnosis, the authors did not mention the occurrence of mediastinal emphysema in diabetic ketoacidosis, which was described in 4 patients by Beigelman and associates1 in 1969. McNicholl and associates2 ascribed the pneumomediastinum to the expiratory effort and grunting associated with ketotic hyperventilation. Munsell3 reviewed 28 cases of spontaneous pneumomediastinum and suggested that an acute transient respiratory obstruction, such as that produced by Valsalva maneuver, cough, emesis, or asthma, was the precipitating factor. Why doesn't mediastinal emphysema develop in a marathon runner during a long-distant run? In this situation, the breathing is normal and brain center–dependent, and it is tapered when the exertion becomes intolerable. (The marathoner is also presumably physically fit and healthy.4) In contrast, in diabetic ketoacidosis, the Kussmaul respiration is involuntary and independent of the respiratory center and abnormally expands lung air spaces, causes alveolar rupture, and results in pneumothorax. As the pulmonary and intrathoracic pressures increase, the extra-alveolar air slips through the periadventitial tissue to the mediastinum, subcutaneous tissue, and other anatomic areas. The incidence of pneumomediastinum complicating diabetic ketoacidosis is low.5-18 Cases are still anecdotal and are sporadically published as one or a few case reports; they are most likely underestimated because the symptom of breathlessness tends to be overshadowed by hyperventilation in diabetic ketoacidosis. Occasionally, Continue reading >>

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